Week 4 - CR Response to Exercise Flashcards
ATP: what is it, what’s released during hydrolysis, how much do we store, + how long it sustains function
- An energy rich compound for biological work.
- Energy released during hydrolysis of ATP
- Store very little (250g)
- Sustains resting func. for 90s + 60s exercise.
ATP + H20 –>
ADP + Pi + H+ + 7kcaloffreeenergy/mol
ADP + H20 –>
AMP + Pi + H+ + 7kcaloffreeenergy/mol
ATP-CP Pathway
(Anaerobic)
-Fuel: stored phosphagens
-Speed of ATP mobilisation: very fast (4 mol ATP/min)
-Capacity: Very Limited
Phosphocreatine -> PO + Creatine + energy
ADP + P + Energy = ATP
Glycolysis
(Anaerobic)
-Fuel: Glycogen/glucose
-Speed of ATP mobilisation: Fast (2.5 mol ATP/min)
- Capacity: Limited
Glycogen -> pyruvic acid -> lactic acid (if O2 isn’t present)
Oxidative phosphorylation
(Aerobic)
- Fuel: Glycogen, glucose, fats, proteins
- Speed of mobilisation: Slow (1 mol ATP/min)
- Capacity: Unlimited
What energy pathway do we use at the beginning of activity + after that?
- The first 30sec. we use ATP-CP
- After: begin to use anaerobic glycolysis
- Lastly: Aerobic pathway-oxidative phosphorylation
- In reality : all 3 are active @ any time but to diff. degrees
Oxygen Consumption (VO2)
The amount of O2 taken up by the lungs
Cellular Oxygen Consumption (QO2)
The amount of oxygen taken up/consumed by the cells (i.e. skeletal muscle cells)
Maximal V02 (V02 max)
The maximal volume of oxygen that a body can take up and use.
What influences V02 max?
Age, intensity/volume of training, gender, mode of activity, environment(altitude/TM v trail), state of physical health, genetics (heart size/muscle type)
Fick Principle equation
VO2max = Q(max) x (Ca02 - CV02)max
Q= cardiac output
Difference on the contents of O2 in the arterial + mixed venous blood
(Ventilation) Ve=
Vt x f = 6 L/min
Fick’s law of diffusion
Vgas = (AxD(P1-P2)) / T A = surface area D= diffusion constant Partial pressure T = Thickness of alveoli capillary membrane
Affect of thickness of alveoli capillary membrane
- Thin makes it easier for diffusion
- Thicker in situations w/ fibrosis in membrane, could even happen w/ intense exercise due to pulm. oedema, inflamm., inhale of dust
VO2 + Ve during 5 min. of moderate intensity exercise
Both ventilation + Vo2 are steady at rest, increase during exercise, then goes down during recovery
Factors that influence breathing during exercise
- Respiratory center (situated in medulla/pons)
(1) gets inputs from the brain (relies on receptors)
(2) Sends info to phrenic nerve to make diaphragm/accessory muscles to contract
(increases VT + RR)
Peripheral chemoreceptors: what do they do + what can it identify
- Carotid bodies pick up low levels of O2 below 60mmHg + increased levels of CO2 or lactic acid
- Important in picking up hypoxemia (low oxygen) + metabolic acidosis
Central chemoreceptors: what is it + what can it identify
Brain; Neurons dotted around respiratory centre; important in picking up H20 ions due to an increase in C02
- Respiratory acidosis
What signals govern the Ve response to constant workload exercise?
I - Central command (brain warns body were exercising)
II - Short-term potentiation (stimulates neurons after resp. Centre is activated)
III - POSSIBLY Chemoreceptors in muscle, mechanoreceptors
- def not carotid bodies b/c O2 doesn’t drop enough, + CO2 doesn’t rise enough for it to be.
What signals govern the Ve response during incremental exercise?
- pH rises, CO2 + O2 decreases –> so pH is what’s really changing ventilation during incremental exercise
What increases ventilation at the end of a submax test (after ventilatory threshold)?
It is driven by carotid bodies (peripheral chemoreceptors) b/c build up of lactic acid, needs the carotid body to bring in the last bit of O2 to finish the aerobic work.
Role of the cardiorespiratory
- Deliver adequate oxygen + remove waste products from tissues.
- Transport nutrients
- Regulate temperature
Cardiac output (Q)
HR x SV (stroke volume)
What is HR controlled by?
Autonomic nerves + circulating catecholamines
- Parasympathetic NS brings the HR down
- Sympathetic NS increases heart rate (doesn’t play much at rest)
What does stroke volume (SV) depend on?
Preload, contractility, + afterload
SV - Preload- what is it / what happens that affects contraction
Degree of stretch prior to contraction (diastole)
- Extra blood stretching cardiomyocytes during period of diastole evokes a stronger contraction.
- They like extra blood coming to heart = stretch in sarcomere length (actin/myosin) = greater contraction
- Troponin becomes more sensitive to Ca++
SV - Contractility
Influenced by sympathetic nerve activity + frank-starling mechanism
- Increased during exercise: increase in sympathetic nerve activity, increase in catecholamines, increased HR
Inotropy
Changes in contractility; + inotropes help stimulate the heart
Sympathetic hormones that are released from the body during exercise:
- These help contract the heart more strongly:
(1) Catecholamines: adrenaline/noradrenaline
(2) B-agnosists (B-antagonist/blockers are inotropes)
Catecholamines bind to beta-receptors in cardiac muscle + increase Ca+ in the muscle which in turn means a stronger contraction.
SV - Afterload
BP = Q x TPR (total peripheral resistance)
Vagal withdrawal
happens at HR up to 100 bpm
Sympathetic drive
- Neural drive supplemented by circulating catecholamines
- HR over 100 bpm
HRR
Heart rate recovery
- Vagal is the initial response & sympathetic comes into play later
What cause an increase in stroke volume during exercise?
EDV - venoconstriction, skeletal muscle pump, respiratory pump
Skeletal / respiratory muscle pumps contribution to increased diastolic volume:
- The compressive effect of muscle contraction pushes blood toward the heart (skeletal muscle pump)
- Reduction in intrapleural pressure during inspiration draws blood towards the heart.
Vasodilatory influences (skeletal muscle)
increased H+ / lactate, increased K+, increased Co2, decreased O2
MAP =
DAP + 1/3 PP
- DAP is dependent on changes in TPR (decreased TPR = vasodilate)
- Increased contractility/SV = increased SAP
Training + VO2 - Central adjustments
Increased cardiac output / SV
- Increased contraction strength, increased EDV (increase filling time, plasma volume, ventricular volume)
- Decreased TPR
Training + VO2 - Peripheral adjustments
Increase muscle blood flow
- Skeletal muscle O2 extraction is increased by:
(1) increases capillary density
(2) increase in myoglobin
(3) increase in size + # of mitochondria
(4) increase in levels of oxidative enzymes
What can affect SpO2 measurements?
Scarring, movement, nail polish, bright light on the probe, poor perfusion
- want 2 surfaces close to parallel
- line measuring HR should be nice + steady
Systolic
Degree of force when heart is contracting (how hard blood is pushing against artery walls, while ventricles squeeze and push blood to the rest of your body)
Diastolic
Degree of force when the heart relaxes (ventricles refill with blood)
Total peripheral resistance
vasoconstriction/vasodilation
What does SpO2 measure?
% of haemoglobin that is bound w/ O2 in blood
- indicates the oxygen carrying capacity of blood.
Considerations when taking BP
- avoid caffeinated/alcoholic beverages 30 min. beforehand.
- Sit quietly for 5 min. w/ back supported /legs uncrossed
- Support arm so elbow is @ or near heart level
- Wrap cuff over bare skin.
- Don’t talk during measurement
Blood Pressure
The pressure exerted by blood against the tunica interna (inner wall of an artery)
Factors that can affect BP
- cuff is too small
- cuff used over clothing
- arm/back/feet unsupported
- emotional state
- talking
- smoking
- alc/caffeine
- temp.
- full bladder
- dehydration
- time of day
What signals govern the increase in Q during constant workload exercise
(1) Vagal withdrawal/ central command/ muscle pump/ sensory nerve activity
(2) Vasodilation in active muscles, stimulation of CV system
(3) baroreflex stabilization of BP
